From Santa Fe Institute Events Wiki
Revision as of 21:48, 12 June 2008 by RobMills
This is the working space for our project. Everything written is a work in progress.
- Evolution of modularity in a host-pathogen system
- Modularity: a pathogen's answer to host interactions
- Do host-pathogen interactions lead to the adaptive evolution for modularity?
- more here
- Does modularity in pathogen genes responsible for an interaction with a host increase its ability to adapt to a host?
- under what conditions does pathogen modularity arise? specifically,
- Is modularity in the host required?
- what configurations of the interaction matrix?
- what influence does population structure have (in the hosts)?
- additional ones here
Questions to answer in proposal
- why are we studying host-pathogen interactions?
- what evidence suggests that modular allelic dependencies might be advantageous in such a host-pathogen system?
- give a one-line description of this type of modularity
- what conditions do we aim to test to show a benefit to modular dependencies/interaction structures?
- what are our null models, i.e. why is (this) result a surprise?
- what impact does this have for the understanding of host-pathogen interactions, and evolvability in general?
Discrete or continuous?
- Pros for discrete: easier to run iterated simulations; possible to run experiments on explicit graph structures
- Pros for continuous: mathematical derivations cleaner
I'm quite sure that there is some overloading here; but these are the types of modularity that have come up in our discussions:
- Modularity for reassortment (Molly)
- Modularity for independence (Molly) (I call this 'functional decomposition' - Rob)
- Repeated modularity: eg where a body segment occurs many times in an organism (Rob)
- Modularity for robustness to antagonistic pleiotrophy (Molly)
- Epitope : the phenotype of a pathogen that interacts with a host
- only need to consider a portion of the host's genome since the pathogen only targets a specialised portion of that genome.